Urinary kallikrein and kinin and plasma bradykinin were measured in normal subjects and in patients with hypertension, Bartter's syndrome, and scleroderma on controlled intakes of sodium, potassium and fluid. Plasma bradykinin in normal subjects is responsive to changes in posture and sodium intake and correlates with the level of plasms renin activity, but not to the level of sodium-retaining steroid. Urinary kallikrein increases with the level of sodium retaining steroid and highly correlated with aldosterone excretion in all studies but urinary kinin excretion is not affected by changes in urinary kallikrein or the level of sodium retaining steroids. Prostaglandin synthetase inhibition decreased urinary kallikrein but had no effect on plasma or urinary kinins. Large changes in ECF volume had no effect on plasma or urinary kinins. Patients with Bartter's syndrome have significantly elevated basal urinary kallikrein and plasma bradykinin but subnormal urinary kinin excretion. During prostaglandin synthesis inhibition urinary kallikrein and plasma bradykinin decreased while urinary kinin excretion increased toward normal. These data indicate an involvement of the kallikrein-kinin system in this syndrome and its relationship to other vasoactive systems. BIBLIOGRAPHIC REFERENCES: Hial, V., Keiser, H. R., and Pisano, J. J. Origin and content of methionyl-lysyl-bradykinin, lysyl-bradykinin and bradykinin in human urine. Biochem. Pharamacol. 25: 2499-2503, 1976. Zinner, S. H., Margolius, H. S., Posner, B., Keiser, H. R., Kass, E. H. Familial aggregation of urinary kallikrein concentration in childhood: relation to blood pressure, race and urinary electrolytes. Amer. J. Epidem. 104: 124-132, 1976.